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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:697.)
© 2007 American Heart Association, Inc.

Editorials

Two Views on Plaque Rupture

Göran K. Hansson; Donald D. Heistad

From the Center for Molecular Medicine (G.K.H.), Department of Medicine, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden; and the University of Iowa Carver College of Medicine and VA Medical Center (D.D.H.), Iowa City, Ia.

Correspondence to Göran K. Hansson, Center for Molecular Medicine L8:03, Karolinska Hospital, SE-171 76, Stockholm, Sweden. E-mail Goran.Hansson@cmm.ki.se

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Plaque rupture probably is the most important cause of myocardial infarction. Plaque rupture is thought to be precipitated by proteases that attack a weakened fibrous cap overlying an inflamed atherosclerotic plaque. Obviously, plaque rupture is of major interest for atherosclerosis researchers and a major target for development of therapy in the pharmaceutical and biotechnology industries.

See pages 705 and 714

There is an urgent need for good models to study plaque rupture in our laboratories. Studies of gene-targeted mice that model atherosclerosis in humans have led to in-depth understanding regarding the initiation and progression of atherosclerosis. In contrast, studies of plaque activation, rupture, and thrombosis have been hampered by a paucity of animal models. Histopathologic analyses of human lesions, largely from autopsy material, have provided important data on cellular properties and histochemical composition of ruptured plaques. These data are of great importance, but they cannot substitute for experimental models that permit investigators to intervene in the pathological process in a controlled fashion.

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Christopher Jackson and his colleagues review their development of a mouse model for plaque instability and rupture.¹ They have found that the brachiocephalic artery (also known as the innominate artery) of hypercholesterolemic mice contains atherosclerotic plaques with histopathologic features that are suggestive of plaque instability and, in some cases, overt rupture. They have presented their evidence for plaque instability and rupture at this site in a series of original articles published in ATVB and elsewhere, and now summarize . . . [Full Text of this Article]

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